ABDOMINAL COMPARTMENT SYNDROME

Intra-abdominal Hypertension and Compartment Syndrome in the Trauma Patient: Is Your Patient at Risk? John J. Gallagher MSN, RN, CCNS, CCRN, RRT Trauma Program Coordinator/Clinical Nurse Specialist Hospital of the University of Pennsylvania

Objective Brief review of pathophysiology Definitions of IAH/ACS Define the risk in trauma patients IAP measurement Prevention and treatment strategies

World Society of Abdominal Compartment Syndrome Guidelines 2013

www. WSACS.org

The Continuum

IAH

ACS

Keys to Success Early Identification of Patients at Risk Early/Ongoing Assessment – IAP (Bladder Pressure Measurement)

Early Therapeutic Intervention – Non-surgical – Surgical

Shock Inability of the cells to meet their metabolic demands • Reductions in Oxygen Delivery • Increases in Oxygen Utilization • Combination of Both • • • • • •

O2 deprivation (oxygen debt) Cellular acidosis

Cellular dysfunction Cellular death Organ dysfunction Organ failure

Trauma/Injury Trigger Hemorrhage Shock - I.V. Fluid - Packing Visceral ischemia - Manipulation Reperfusion edema

Visceral edema

IAH/ ACS

Inflammatory Response “Two Hit Theory” Primary Insult (trauma)

Secondary Insult (shock)

Inflammatory Response

CAPILLARY LEAK

INTRA-ABDOMINAL TISSUE EDEMA

Photo by John Gallagher

4 Risk Factor Categories Reduced Abdominal Wall Compliance

Capillary Leak/ Fluid Resuscitation

Increased Abdominal Contents

Increased Intraluminal Contents

World Society of Abdominal Compartment Syndrome

Risk Factors

Clinical Scenarios Abdomen closed post-op Temporary abdominal closure Volume Resuscitation/Massive Transfusion Lethal Triad (acidosis, coagulopathy, hypothermia) Damage control stage 4 (closure)

Damage Control Laparotomy Stage 1

•Control of hemorrhage •Control of contamination Stage 2 •Rewarming

•Packing •Temp closure

•Correct coagulopathy

Stage 4

•Ventilation

•Abdominal Reconstruction

•Hemodynamics Stage 3 •Re inspection •Definitive injury repair •Abdominal Closure

Reduced Abdominal Wall Compliance   

Closure of the abdomen post-laparotomy Burns to the thoraco-abdominal wall Temporary abdominal closure









Abdominal Bedside Tote


Bogota/Silo Bag Closure

trauma.org Image Bank

Burn Injury

•Hershberger et al. (2007) Journal of Burn Care Research •Ennis et al. (2008) Journal of Trauma •Ball et al. (2006) Journal of Trauma

Capillary Leak/Fluid Resuscitation SHOCK • Inflammatory Response • Capillary Leak

Lethal Triad

Coagulopathy • Crystalloid Resuscitation • Massive Transfusion

Increased Abdominal Contents • Hemoperitoneum • Burns (ascites)

Increase Intraluminal Contents Ileus Gastroparesis Obstructions

Intra-abdominal Pressure Variations Normal: 5 – 7mmHg – Normal in Obesity: 9 – 14 mmHg

HOB elevation: 2 - 5 mmHg above baseline

PEEP > 15 mmHg – Most profound when IAP is > 12mmHg baseline

Intra abdominal Hypertension A pathologic elevation of intra-abdominal pressure – Sustained or reproducible IAP > 12 mmHg

Intra abdominal Hypertension IAP > 12mmHg Grade I: 12 - 15 mmHg Grade II: 16 – 20 mmHg Grade III: 21 -25 mmHg Grade IV: > 25 mmHg World Society of the Abdominal Compartment Syndrome

Abdominal Perfusion Pressure (APP)

APP= MAP- IAP Target APP > 60 mmHg APP < 50 mmHg is associated with increased mortality

Pediatric Considerations Lower MAP and lower threshold for hypoperfusion IAH and ACS occur at lower IAP – ACS is IAP of > 10 mmHg with new onset organ dysfunction Ejike et al (2008) Critical Care Medicine

Abdominal Compartment Syndrome An increase in intra-abdominal pressure that exceeds the capacity of the compartment, resulting in the impaired perfusion and function of multiple organ systems

Abdominal Compartment Syndrome Presence of both…. IAP > 20 mm Hg Regardless of APP New onset single/multiple organ system failure

Abdominal Compartment Syndrome Primary Secondary Recurrent

Primary Abdominal Compartment Syndrome Associated with injury or disease in the abdominopelvic region


Secondary Abdominal Compartment Syndrome Develops from conditions outside the abdomen –Massive fluid resuscitation –Burns –Sepsis

SACS Post Injury Lower SBP Penetrating chest Vascular Injuries Multiple extremity fractures

Secondary Abdominal Compartment Syndrome Inflammatory process that may be more subtle – Trauma: » SACS represents 58% of post injury ACS » 38 – 68 % mortality

Resuscitation outside the OR – IR and ICU – More crystalloid – Longer times to control of bleeding

22 y.o. unrestrained driver, ejected in a MVC: – Unresponsive – Heart rate: 130 – Blood pressure: 80/50 mmHg

L. hemothorax- 750 ml from the chest tube Abdominal ultrasound positive for fluid LUQ Taken to OR for splenectomy Admitted to the SICU

22 y.o. male post MVC transferred into the SICU after progressive hemodynamic deterioration BP 90/50 HR 122 T 102°F Sat 88% Pale, diaphoretic

Breathing becomes labored, mental status decreases – Intubated – Central line placed »CVP is 3 mm Hg – Urinary catheter placed » 200 ml dark urine

4 liters additional LR is infused – MAP: 60, HR: 110, CVP: 10, – Urine output: 15 ml/hr •

Norepinephrine started – MAP: 65, HR 116, CVP 11 – Urine output 20 ml for last 2 hours Bladder pressure monitoring device attached:

Would you give this patient volume? • IAP 30 mmHg

Recurrent Abdominal Compartment Syndrome Abdominal Compartment Syndrome that re-develops after previous medical or surgical treatment

Recurrent Abdominal Compartment Syndrome Can develop even with an “expanded” (open) abdomen with temporary closure Increased morbidity and mortality

Gracias, V.H. et al. 2002. Archives of Surgery

Open Abdomen

Expanded Abdomen

Dynamic Tension

Organ Systems Compromised Gastrointestinal Pulmonary Cardiovascular Renal Neurological

Gastrointestinal Effects Increased IAP Compression of mesenteric vessels Gastric mucosal acidosis (pHi) Mesenteric ischemia

Pulmonary Effects Lung expansion

Increased Intra-abdominal pressure

Pressure on Diaphragm

Cardiovascular Effects Increased IAP

Pre-load

Afterload

May occur with IAPs of as low as 10 mmHg

Cardiovascular Assessment Findings Normotensive CVP, PA, PCOP, SVR, PVR C.O.

CVP corrected PCOP corrected

= =

CVP measured

-

PCOP measured

IAP/2

-

IAP/2

Renal Impact of Elevated IAP

Neurologic Effect Increased IAP Reduced venous return from the brain Cerebral hyperemia Increase in ICP

Neurological Manifestations Refractory Intracranial Hypertension Elevated ICPs

CPPs

Brain tissue oxygen

Early/Ongoing Assessment Early Initiation of IAP monitoring in patients with 2 or more risk factors Serial measurement until IAH risk is past

Bladder Pressure Monitoring – The current standard for monitoring IAP

– Comparable to direct intraperitoneal pressure measurements, but is non-invasive (Bailey, Crit Care 2000) – More reliable and reproducible than clinical judgment (Kirkpatrick, CJS 2000; Sugrue World J Surg 2002)

Intra-Abdominal Pressure Measurement Performed in the supine position Zero at the level of the mid-axillary line (pelvis) Expressed in mmHg (1 mmHg= 1.36 cmH2O) Measured at End-expiration Measure 30 – 60 sec after instillation of saline

The correct transducer position at the iliac crest in the mid-axillary line in the supine position and with head of bed elevation.

Transducer location


Instilled Fluid Volume Adults – No greater than 25 ml of saline

Children – 3ml minimum volume – 1 ml/kg for children up to 25

Considerations Neurogenic or contracted bladder Injuries to the bladder HOB elevations

AbViser® Intra-Abdominal Pressure Monitoring Kit

Manometry Measurement

Foley Manometer Holtech Medical

Modified Pressure Monitor System

Bladder Pressure Waveform

Keys to Accuracy Standardized measurement device Standardized clinical protocol

Kimball et al. (2007) Intensive Care Medicine

Monitoring Protocols Trigger Conditions

Monitoring System • Frequency of Monitoring • Reporting Thresholds

Criteria for Termination of Monitoring

Ongoing staff proficiency

Pitfalls Failing to identify patients at risk – Temporary abdominal closure – Volume resuscitation – Post-op abdominal closure

Requiring an order to monitor IAP Staff unfamiliar with the monitoring procedure Terminating monitoring too soon

Management Strategies Optimize systemic perfusion/organ function Non-surgical interventions to reduce IAP Surgical decompression

Ventilation Strategies Decreased thoracic compliance Normal lung tissue compliance Lung Protective Strategies – Limit ventilation pressures – Optimize PEEP

Non-surgical Measures Optimize Abdominal Perfusion Pressure (APP) Volume optimize preload

improve cardiac index worsen edema

Vasopressors » Achieve APP > 60 mmHg after euvolemia » Risk of intestinal ischemia

Cardiac Output Stroke Volume Preload

Volume •SV SVV •PPV •EDV •Doppler •Echo

Afterload Resistance •SVR •PVR

X HR Contractility Stroke Work (I) •RVSW •LVSW

Pressure •CVP •PCOP

Images provided by J Gallagher


Improve Abdominal Wall Compliance – Analgesia/Sedation – Remove/Expand Abdominal Closure – Escharotomy (Burn Patients) – Positioning » HOB not greater than 30 degrees » Reverse trendelenberg » Abdomen unsupported while prone

– Neuromuscular Blocking Agents

Correct Positive Fluid Balance Avoid excessive fluid resuscitation Aim for zero/negative fluid balance Diuretics (hemodynamically stable) Colloids/Hypertonic fluids Fluid restriction CRRT

Evacuation of Abdominal Collections U/S and CT guided percutaneous drainage Surgical removal of space occupying lesions •Ascites evacuation •Abscess removal •Hematoma removal

Evacuation of Intraluminal Contents Gastric/Rectal decompression Colonoscopic decompression Gastroprokinetics /Coloprokinetic Correct electrolyte abnormalities – Potassium – Magnesium – Calcium/Phos Maintain enteral nutrition unless progression to ACS

Surgical Treatment Measures Surgical Decompression – IAP > 20 mmHg & organ dysfunction

Removal of packing Drainage of intra-abdominal collections

Conclusions Majority of Critically Ill Patients are AT RISK IAH and ACS increase morbidity, mortality and ICU length of stay Early detection and intervention can reduce these complications in many patients – Monitoring Bladder Pressure key to early detection

Early treatment of IAH with non-surgical strategies can prevent progression to ACS

Resources

World Society of Abdominal Compartment Syndrome www.wsacs.org

Thank You

[email protected]

ABDOMINAL COMPARTMENT SYNDROME

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